Deficiency Diseases

According to J. C. Drummond and Anne Wilbraham (1958), the earliest mention of rickets as a disease entity was made in a 1634 Bill of Mortality for the city of London. Between 1645 and 1650, at least three physicians, including Francis Glisson, gave accounts of the disease. Glisson's work, De rachitide, published in 1650, not only was the most extensive but also made reference to scurvy as a disease that could be associated with rickets in infants. Subsequently, most European pediatric texts discussed rickets, but no clear reference to infantile scurvy reappeared until the late nineteenth century. It would seem that rickets was commonplace in northern Europe, particularly in England, whereas infantile scurvy was rare until the advent of proprietary foods and the use of boiled or sterilized milk. In the United States, however, rickets was either unrecognized or had a low incidence until the late nineteenth century, for it was rarely discussed in the earlier pediatric textbooks or, if mentioned, was dismissed as of rare occurrence (for the first North American monograph on rickets, see Parry 1872).

Thomas Cone and others have pointed out the lack of consensus on the cause of rickets by the end of the nineteenth century (Hess 1929; Cone 1979). Some believed it was due to an improper diet, others to a lack of sunshine or exposure to polluted air. Yet others regarded it as a degenerative disease. In this view, fortified by perceived similarities in the microscopic bony lesions of syphilis and rickets, parental syphilis could be expressed in offspring as rickets or as an increased liability to rickets (for a discussion of "hereditary" syphilis as the cause of other diseases in the offspring of syphilitics, see Lomax 1979).

As indicated by Kenneth Carpenter (1986) ideas about the cause of scurvy were just as confused. In 1883 Thomas Barlow described the clinical and pathological signs of infantile scurvy, a disease entity rarely recognized in babies. He also indicated that the best remedy was orange juice. Soon physicians in other countries were recognizing "Barlow's disease," but they could not agree as to the cause or even the cure. In 1898 the American Pediatric Society reported an investigation of infantile scurvy. Most physicians who had been consulted thought that proprietary foods, and perhaps sterilized milk, were responsible for the condition. One dissenter, August Caillé, considered the illness to be a form of ptomaine poisoning caused by the absorption of toxins (Cone 1979; Carpenter 1986). Epidemiology and clinical medicine could not produce decisive evidence in favor of any particular theory (see Wilson 1975).

Early in the twentieth century, researchers using animal models to establish dietary requirements came to the rescue. Administering modified diets to animals was not a new technique, but with improvements in chemical analysis it was becoming more precise. In 1907 scurvy was produced experimentally in guinea pigs, and further experiments led Casimir Funk to propose, in 1912, that scurvy, pellagra, rickets, and beriberi were caused by a dietary lack of essential factors, which he called "vita-mines." The hypothesis was received with enthusiasm, deficiency diseases were induced in animals, and between 1928 and 1938, vitamins A, B^ C, D, and E were isolated and chemically defined (Harris 1970).

Another type of deficiency was recognized when Cicely Williams (1933) drew attention to kwashiorkor, a disorder brought on by malnutrition in previously healthy West African toddlers after weaning.

Since then, physicians and nutritionists have sought to understand, prevent, and cure this and similar disorders and syndromes, collectively known as protein-energy malnutrition (PEM) and most commonly found in developing countries. (The research literature is very large; see, e.g., Trowell, Davies, and Dean 1954; Jellife 1969; Olson 1975.) At one extreme are marasmic infants, in whom growth failure is combined with wasting from starvation, as a result of a diet deficient in both calories and protein. At the other extreme is kwashiorkor, thought to be due to a diet with an adequate caloric content but deficient in usable protein. In between are less obvious forms of PEM, characterized by growth retardation and associated with a greater liability to infection than is found in well-nourished children. Infectious disease interferes with a child's appetite, thereby provoking or worsening malnutrition, and the latter state decreases resistance to infection. In former centuries, protein-calorie deficiency syndromes were probably responsible for much wasting, infection, and diarrhea in American and European babies, but the incidence would be difficult to estimate retrospectively because illness was perceived and described so differently at that time.

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